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The following commentary on Jang and Choi’s chapter Issues and New Directions in Personality Disorder (PD) Genetics (This Volume) echoes their call to harness advances in PD assessment rather than rely on politically derived "top down" nosologies. We first discuss how recent work in the joint hierarchical structure of PD traits and psychopathology, as well as, personality dynamics (i.e., how personality manifests in different situations) likely offer fruitful avenues for exploring the more nuanced role of genetics in the development and maintenance of PD. Second, we highlight the need to better understand the role of environment in PD genetics and discuss emerging models (e.g., common pathway model). Third, we stress the need for more research and larger samples in order to arrive at stronger conclusions. Fourth, we consider how advances in gene-environment research can help to determine targets for PD prevention and treatment.
Preliminary evidence has suggested that high-fat diets (HFD) enriched with SFA, but not MUFA, promote hyperinsulinaemia and pancreatic hypertrophy with insulin resistance. The objective of this study was to determine whether the substitution of dietary MUFA within a HFD could attenuate the progression of pancreatic islet dysfunction seen with prolonged SFA-HFD. For 32 weeks, C57BL/6J mice were fed either: (1) low-fat diet, (2) SFA-HFD or (3) SFA-HFD for 16 weeks, then switched to MUFA-HFD for 16 weeks (SFA-to-MUFA-HFD). Fasting insulin was assessed throughout the study; islets were isolated following the intervention. Substituting SFA with MUFA-HFD prevented the progression of hyperinsulinaemia observed in SFA-HFD mice (P < 0·001). Glucose-stimulated insulin secretion from isolated islets was reduced by SFA-HFD, yet not fully affected by SFA-to-MUFA-HFD. Markers of β-cell identity (Ins2, Nkx6.1, Ngn3, Rfx6, Pdx1 and Pax6) were reduced, and islet inflammation was increased (IL-1β, 3·0-fold, P = 0·007; CD68, 2·9-fold, P = 0·001; Il-6, 1·1-fold, P = 0·437) in SFA-HFD – effects not seen with SFA-to-MUFA-HFD. Switching to MUFA-HFD can partly attenuate the progression of SFA-HFD-induced hyperinsulinaemia, pancreatic inflammation and impairments in β-cell function. While further work is required from a mechanistic perspective, dietary fat may mediate its effect in an IL-1β–AMP-activated protein kinase α1-dependent fashion. Future work should assess the potential translation of the modulation of metabolic inflammation in man.
Major depressive disorder (MDD) is a common mood disorder, with a heritability of around 34%. Molecular genetic studies made significant progress and identified genetic markers associated with the risk of MDD; however, progress is slowed down by substantial heterogeneity as MDD is assessed differently across international cohorts. Here, we used a standardized online approach to measure MDD in multiple cohorts in the Netherlands and evaluated whether this approach can be used in epidemiological and genetic association studies of depression.
Within the Biobank Netherlands Internet Collaboration (BIONIC) project, we collected MDD data in eight cohorts involving 31 936 participants, using the online Lifetime Depression Assessment Self-report (LIDAS), and estimated the prevalence of current and lifetime MDD in 22 623 unrelated individuals. In a large Netherlands Twin Register (NTR) twin-family dataset (n ≈ 18 000), we estimated the heritability of MDD, and the prediction of MDD in a subset (n = 4782) through Polygenic Risk Score (PRS).
Estimates of current and lifetime MDD prevalence were 6.7% and 18.1%, respectively, in line with population estimates based on validated psychiatric interviews. In the NTR heritability estimates were 0.34/0.30 (s.e. = 0.02/0.02) for current/lifetime MDD, respectively, showing that the LIDAS gives similar heritability rates for MDD as reported in the literature. The PRS predicted risk of MDD (OR 1.23, 95% CI 1.15–1.32, R2 = 1.47%).
By assessing MDD status in the Netherlands using the LIDAS instrument, we were able to confirm previously reported MDD prevalence and heritability estimates, which suggests that this instrument can be used in epidemiological and genetic association studies of depression.
Studies on neighbourhood characteristics and depression show equivocal results.
This large-scale pooled analysis examines whether urbanisation, socioeconomic, physical and social neighbourhood characteristics are associated with the prevalence and severity of depression.
Cross-sectional design including data are from eight Dutch cohort studies (n= 32 487). Prevalence of depression, either DSM-IV diagnosis of depressive disorder or scoring for moderately severe depression on symptom scales, and continuous depression severity scores were analysed. Neighbourhood characteristics were linked using postal codes and included (a) urbanisation grade, (b) socioeconomic characteristics: socioeconomic status, home value, social security beneficiaries and non-Dutch ancestry, (c) physical characteristics: air pollution, traffic noise and availability of green space and water, and (d) social characteristics: social cohesion and safety. Multilevel regression analyses were adjusted for the individual's age, gender, educational level and income. Cohort-specific estimates were pooled using random-effects analysis.
The pooled analysis showed that higher urbanisation grade (odds ratio (OR) = 1.05, 95% CI 1.01–1.10), lower socioeconomic status (OR = 0.90, 95% CI 0.87–0.95), higher number of social security beneficiaries (OR = 1.12, 95% CI 1.06–1.19), higher percentage of non-Dutch residents (OR = 1.08, 95% CI 1.02–1.14), higher levels of air pollution (OR = 1.07, 95% CI 1.01–1.12), less green space (OR = 0.94, 95% CI 0.88–0.99) and less social safety (OR = 0.92, 95% CI 0.88–0.97) were associated with higher prevalence of depression. All four socioeconomic neighbourhood characteristics and social safety were also consistently associated with continuous depression severity scores.
This large-scale pooled analysis across eight Dutch cohort studies shows that urbanisation and various socioeconomic, physical and social neighbourhood characteristics are associated with depression, indicating that a wide range of environmental aspects may relate to poor mental health.
Medical procedures and patient care activities may facilitate environmental dissemination of healthcare-associated pathogens such as methicillin-resistant Staphylococcus aureus (MRSA).
Observational cohort study of MRSA-colonized patients to determine the frequency of and risk factors for environmental shedding of MRSA during procedures and care activities in carriers with positive nares and/or wound cultures. Bivariate analyses were performed to identify factors associated with environmental shedding.
A Veterans Affairs hospital.
This study included 75 patients in contact precautions for MRSA colonization or infection.
Of 75 patients in contact precautions for MRSA, 55 (73%) had MRSA in nares and/or wounds and 25 (33%) had positive skin cultures. For the 52 patients with MRSA in nares and/or wounds and at least 1 observed procedure, environmental shedding of MRSA occurred more frequently during procedures and care activities than in the absence of a procedure (59 of 138, 43% vs 8 of 83, 10%; P < .001). During procedures, increased shedding occurred ≤0.9 m versus >0.9 m from the patient (52 of 138, 38% vs 25 of 138, 18%; P = .0004). Contamination occurred frequently on surfaces touched by personnel (12 of 38, 32%) and on portable equipment used for procedures (25 of 101, 25%). By bivariate analysis, the presence of a wound with MRSA was associated with shedding (17 of 29, 59% versus 6 of 23, 26%; P = .04).
Environmental shedding of MRSA occurs frequently during medical procedures and patient care activities. There is a need for effective strategies to disinfect surfaces and equipment after procedures.
To explore the associations of absolute and relative measures of exposure to food retailers with dietary patterns, using simpler and more complex measures.
Urban regions in Belgium, France, Hungary, the Netherlands and the UK.
European adults (n 4942). Supermarkets and local food shops were classified as ‘food retailers providing healthier options’; fast-food/takeaway restaurants, cafés/bars and convenience/liquor stores as ‘food retailers providing less healthy options’. Simpler exposure measures used were density of healthy and density of less healthy food retailers. More complex exposure measures used were: spatial access (combination of density and proximity) to healthy and less healthy food retailers; density of healthier food retailers relative to all food retailers; and a ratio of spatial access scores to healthier and less healthy food retailers. Outcome measures were a healthy or less healthy dietary pattern derived from a principal component analysis (based on consumption of fruits, vegetables, fish, fast foods, sweets and sweetened beverages).
Only the highest density of less healthy food retailers was significantly associated with the less healthy dietary pattern (β = −129·6; 95 % CI −224·3, −34·8). None of the other absolute density measures nor any of the relative measures of exposures were associated with dietary patterns.
More complex measures of exposure to food retailers did not produce stronger associations with dietary patterns. We had some indication that absolute and relative measures of exposure assess different aspects of the food environment. However, given the lack of significant findings, this needs to be further explored.
The main focus is on the assessment of the effects of early institutional care and compares three longitudinal studies from Romania, Greece and Hong Kong/China. The findings have been strikingly contrasting. The review asks if the risks are dependent on whether or not the institutional rearing is accompanied by gross pervasive deprivation (as it was in Romania) and investigates the methodological issues to explore the causal influence of the outcomes. Evidence is considered on changing institutional practices and the benefits of doing so. Comparison is made between institutions with major deprivation and those without global deprivation. A small number of studies are discussed that look at direct comparisons between institutional and community care. The empirical and conceptual implications of the findings are discussed.
Seasonal respiratory illnesses present a major burden on primary care services. We assessed the burden of respiratory illness on a national telehealth system in England and investigated the potential for providing early warning of respiratory infection. We compared weekly laboratory reports for respiratory pathogens with telehealth calls (NHS 111) between week 40 in 2013 and week 29 in 2015. Multiple linear regression was used to identify which pathogens had a significant association with respiratory calls. Children aged <5 and 5–14 years, and adults over 65 years were modelled separately as were time lags of up to 4 weeks between calls and laboratory specimen dates. Associations with respiratory pathogens explained over 83% of the variation in cold/flu, cough and difficulty breathing calls. Based on the first two seasons available, the greatest burden was associated with respiratory syncytial virus (RSV) and influenza, with associations found in all age bands. The most sensitive signal for influenza was calls for ‘cold/flu’, whilst for RSV it was calls for cough. The best-fitting models showed calls increasing a week before laboratory specimen dates. Daily surveillance of these calls can provide early warning of seasonal rises in influenza and RSV, contributing to the national respiratory surveillance programme.
Deaths in England attributable to pandemic (H1N1) 2009 deaths were investigated through a mandatory reporting system. The pandemic came in two waves. The second caused greater population mortality than the first (5·4 vs. 1·6 deaths per million, P<0·001). Mortality was particularly high in those with chronic neurological disease, chronic heart disease and immune suppression (450, 100, and 94 deaths per million, respectively); significantly higher than in those with chronic respiratory disease (39 per million) and those with no risk factors (2·4 per million). Greater mortality in the second wave has been observed in all previous influenza pandemics. This time, the explanation appears to be behavioural. This emphasizes the importance of maintaining public and clinical awareness of risks associated with pandemic influenza beyond the initial high-profile period.
Uncertainties exist regarding the population risks of hospitalization due to pandemic influenza A(H1N1). Understanding these risks is important for patients, clinicians and policy makers. This study aimed to clarify these uncertainties. A national surveillance system was established for patients hospitalized with laboratory-confirmed pandemic influenza A(H1N1) in England. Information was captured on demographics, pre-existing conditions, treatment and outcomes. The relative risks of hospitalization associated with pre-existing conditions were estimated by combining the captured data with population prevalence estimates. A total of 2416 hospitalizations were reported up to 6 January 2010. Within the population, 4·7 people/100 000 were hospitalized with pandemic influenza A(H1N1). The estimated hospitalization rate of cases showed a U-shaped distribution with age. Chronic kidney disease, chronic neurological disease, chronic respiratory disease and immunosuppression were each associated with a 10- to 20-fold increased risk of hospitalization. Patients who received antiviral medication within 48 h of symptom onset were less likely to be admitted to critical care than those who received them after this time (adjusted odds ratio 0·64, 95% confidence interval 0·44–0·94, P=0·024). In England the risk of hospitalization with pandemic influenza A(H1N1) has been concentrated in the young and those with pre-existing conditions. By quantifying these risks, this study will prove useful in planning for the next winter in the northern and southern hemispheres, and for future pandemics.
Data from a representative community sample were used to explore predictors of lifetime suicidality and to examine associations between distal adolescent and more proximal adult risks.
Data are from a midlife follow-up of the Isle of Wight study, an epidemiological sample of adolescents assessed in 1968. Ratings of psychiatric symptoms and disorder, relationships and family functioning and adversity were made in adolescence; adult assessments included lifetime psychiatric history and suicidality, neuroticism and retrospective reports of childhood sexual abuse and harsh parenting.
A wide range of measures of childhood psychopathology, adverse experiences and interpersonal difficulties were associated with adult suicidality; associations were particularly strong for adolescent irritability, worry and depression. In multivariate analyses, substantial proportions of these effects could be explained by their association with adult psychopathology and neuroticism, but additional effects remained for adolescent irritability and worry.
Factors of importance for long-term suicidality risk are evident in adolescence. These include family and experiential adversities as well as psychopathology. In particular, markers of adolescent worry and irritability appeared both potent risks and ones with additional effects beyond associations with adult disorder and adult neuroticism.
There have been numerous exhortations for more ‘translational research’. A selective review of historical examples of research leading to health benefits is used to consider the various forms of successful interplay between basic science and clinical applications. This is followed by a consideration of key neuroscience findings that might be relevant for translation, and then by a discussion of the challenges and opportunities in relation to mental disorders. The time-frame for the pathway from science findings to health benefits is usually long, and generally requires an interactive interplay among different scientific strategies. There is a false dichotomy between so-called basic and applied research and translation needs to proceed from the bedside to the laboratory as well as in the opposite direction. There is a key need for bridging research of the hypothesis-testing experimental medicine variety. Health benefits may involve either public health considerations or the treatment of individual patients, or both. There are now some opportunities for direct translational research but there is a much greater need for hypothesis-based bridging studies that occupy a crucial mid-phase in the pathway from science findings to health benefits.
There is increased interest in assessing the family history of psychiatric disorders for both genetic research and public health screening. It is unclear how best to combine family history reports into an overall score. We compare the predictive validity of different family history scores.
Probands from the Dunedin Study (n=981, 51% male) had their family history assessed for nine different conditions. We computed four family history scores for each disorder: (1) a simple dichotomous categorization of whether or not probands had any disordered first-degree relatives; (2) the observed number of disordered first-degree relatives; (3) the proportion of first-degree relatives who are disordered; and (4) Reed's score, which expressed the observed number of disordered first-degree relatives in terms of the number expected given the age and sex of each relative. We compared the strength of association between each family history score and probands' disorder outcome.
Each score produced significant family history associations for all disorders. The scores that took account of the number of disordered relatives within families (i.e. the observed, proportion, and Reed's scores) produced significantly stronger associations than the dichotomous score for conduct disorder, alcohol dependence and smoking. Taking account of family size (i.e. using the proportion or Reed's score) produced stronger family history associations depending on the prevalence of the disorder among family members.
Dichotomous family history scores can be improved upon by considering the number of disordered relatives in a family and the population prevalence of the disorder.
Ian Snape, Contaminants Geochemist Working for the Australian Antarctic Division in Tasmania,
Larry Acomb, Geosphere Inc., 3055 Seawind Drive, Anchorage AK 99516, USA,
David L. Barnes, Dept. of Civil and Environmental Engineering, University of Alaska Fairbanks, PO Box 755900, Fairbanks AK 99775, USA,
Steve Bainbridge, Contaminated Sites Program, Division of Spill Prevention and Response, Department of Environmental Conservation, 610 University Avenue, Fairbanks AK 99709–3643, USA,
Robert Eno, Department of Sustainable Development, Government of Nunavut, PO Box 1000, Stn 1195, Iqaluit NU X0A 0H0, Canada,
Dennis M. Filler, Dept. of Civil and Environmental Engineering, University of Alaska Fairbanks, PO Box 755900, Fairbanks AK 99775, USA,
Natalie Plato, Department of Sustainable Development, Government of Nunavut, PO Box 1000, Stn 1195, Iqaluit NU X0A 0H0, Canada,
John S. Poland, Analytical Services Unit, Queens University, Kingston ON K7L 3N6, Canada,
Tania C. Raymond, Environmental Protection and Change Program, Australian Antarctic Division, Channel Highway, Kingston, Tasmania 7050, Australia,
John L. Rayner, Environmental Protection and Change Program, Australian Antarctic Division, Channel Highway, Kingston, Tasmania 7050, Australia,
Martin J. Riddle, Environmental Protection and Change Program, Australian Antarctic Division, Channel Highway, Kingston, Tasmania 7050, Australia,
Anne G. Rike, Dept. of Environmental Technology, Norwegian Geotechnical Institute, PO Box 3930, Ullevaal Stadion, N-0806 Oslo, Norway,
Allison Rutter, Analytical Services Unit, Queens University, Kingston ON K7L 3N6, Canada,
Alexis N. Schafer, University of Saskatchewan, 51 Campus Drive, Saskatoon, Canada S7N 5A8,
Steven D. Siciliano, University of Saskatchewan, 51 Campus Drive, Saskatoon SK S7N 5A8, Canada,
James L. Walworth, Dept. of Soil Water and Environmental Science, University of Arizona, 429 Shantz Bldg. #38, Tucson AZ 85721, USA
Oil and fuel spills are among the most extensive and environmentally damaging pollution problems in cold regions and are recognized as potential threats to human and ecosystem health. It is generally thought that spills are more damaging in cold regions, and that ecosystem recovery is slower than in warmer climates (AMAP 1998; Det Norske Veritas 2003). Slow natural attenuation rates mean that petroleum concentrations remain high for many years, and site managers are therefore often forced to select among a range of more active remediation options, each of which involves a trade-off between cost and treatment time (Figure 11). The acceptable treatment timeline is usually dictated by financial circumstance, perceived risks, regulatory pressure, or transfer of land ownership.
In situations where remediation and site closure are not urgent, natural attenuation is often considered an option. However, for many cold region sites, contaminants rapidly migrate off-site (Gore et al. 1999; Snape et al. 2006a). In seasonally frozen ground, especially in wetlands, a pulse of contamination is often released with each summer thaw (AMAP 1998; Snape et al. 2002). In these circumstances natural attenuation is likely not a satisfactory option. Simply excavating contaminants and removing them for off-site treatment may not be viable either, because the costs are often prohibitive and the environmental consequences of bulk extraction can equal or exceed the damage caused by the initial spill (Filler et al. 2006; Riser-Roberts 1998).